Parasitology

Research Article

Transcriptome analysis of Schistosoma mansoni larval development using serial analysis of gene expression (SAGE)

A. S. TAFTa1, J. J. VERMEIREa1a3, J. BERNIERa2, S. R. BIRKELANDa2, M. J. CIPRIANOa2, A. R. PAPAa2, A. G. McARTHURa2 and T. P. YOSHINOa1 c1

a1 Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2115 Observatory Drive, Madison, WI, USA

a2 Josephine Bay Paul Center for Comparative Molecular Biology and Evolution, Marine Biological Laboratory, Woods Hole, MA, USA

a3 Current address: Department of Pediatrics, Yale University School of Medicine, New Haven, CT, USA.

SUMMARY

Infection of the snail, Biomphalaria glabrata, by the free-swimming miracidial stage of the human blood fluke, Schistosoma mansoni, and its subsequent development to the parasitic sporocyst stage is critical to establishment of viable infections and continued human transmission. We performed a genome-wide expression analysis of the S. mansoni miracidia and developing sporocyst using Long Serial Analysis of Gene Expression (LongSAGE). Five cDNA libraries were constructed from miracidia and in vitro cultured 6- and 20-day-old sporocysts maintained in sporocyst medium (SM) or in SM conditioned by previous cultivation with cells of the B. glabrata embryonic (Bge) cell line. We generated 21 440 SAGE tags and mapped 13 381 to the S. mansoni gene predictions (v4.0e) either by estimating theoretical 3′ UTR lengths or using existing 3′ EST sequence data. Overall, 432 transcripts were found to be differentially expressed amongst all 5 libraries. In total, 172 tags were differentially expressed between miracidia and 6-day conditioned sporocysts and 152 were differentially expressed between miracidia and 6-day unconditioned sporocysts. In addition, 53 and 45 tags, respectively, were differentially expressed in 6-day and 20-day cultured sporocysts, due to the effects of exposure to Bge cell-conditioned medium.

(Received November 30 2008)

(Revised January 16 2009)

(Accepted January 16 2009)

(Online publication March 06 2009)

Correspondence:

c1 Corresponding author: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2115 Observatory Drive, Madison, WI, 53726, USA. Tel: +608 263 6002. Fax: +608 265 8122. E_mail: yoshinot@svm.vetmed.wisc.edu

Footnotes

† These authors contributed equally to this work.

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